Tobacco Use and Your Teeth

Tobacco use has been recognized to be a significant risk factor for the development and progression of periodontal disease. Its use is associated with increased pocket depths, loss of periodontal attachment, alveolar bone and a higher rate of tooth loss. Nicotine, a major component and most pharmacologically active agent in tobacco is likely to be a significant contributing factor for the exacerbation of periodontal diseases. Available literature suggests that nicotine affects gingival blood flow, cytokine production, neutrophil and other immune cell function; connective tissue turnover, which can be the possible mechanisms responsible for overall effects of tobacco on periodontal tissues. Inclusion of tobacco cessation as a part of periodontal therapy encourages dental professionals to become more active in tobacco cessation counseling. This will have far reaching positive effects on our patients’ oral and general health.

Tobacco use in any form has the potential to profoundly alter the systemic and oral health of the individual. The use of tobacco is associated with a wide spectrum of disease including stroke, coronary artery disease, peripheral artery disease, gastric ulcer and cancers of mouth, larynx, esophagus, pancreas, bladder and uterine cervix. It is also a major cause of chronic obstructive pulmonary disease and risk factor for low birth weight babies. It has also been recognized to be a significant risk factor for periodontitis affecting the prevalence, extent and severity of disease. Tobacco use is associated with increased pocket depths, loss of periodontal attachment, alveolar bone and higher rate of tooth loss. In addition, it may influence the clinical outcome of non surgical and surgical therapy as well as long term success of implant placement.

Pindborg (1947) was one of the first investigators to study the relationship between smoking and periodontal disease. He discovered a higher prevalence of acute necrotizing ulcerative gingivitis. Early studies show that smokers had higher levels of periodontitis but they also had poorer levels of oral hygiene and higher levels of calculus

1. Effects of smoking on periodontal disease

The relationship between smoking and periodontal diseases has been studied extensively over the past 15 years and both cross-sectional and longitudinal studies provide strong epidemiologic evidence of a positive association between smoking and clinical and radiographic signs of periodontitis, as well as an increased risk of periodontitis in smokers, In a 10-year longitudinal radiographic study of alveolar bone loss, smoking was a significant predictor of future bone loss in those subjects who had at least 20 teeth at the beginning of the study. In a five-year study of attachment loss in 800 community dwelling adults, smokers were found to be at an increased risk of attachment loss. In a further 12-month longitudinal study, smokers were shown to be at significantly greater risk for attachment loss than nonsmokers, the odds ratio being quoted as 5.4. In one of the largest studies of risk factors for periodontal disease with 1361 subjects from Erie County, NY, aged 25–74 years; it was shown that smokers were at greater risk of experiencing severe bone loss than nonsmokers, with odds ratios ranging from 3.25 to 7.28 for light and heavy smokers, respectively.

A study of 540 Swedish adults 20–70 years of age has revealed that three variables – smoking, greater age and higher mean plaque levels – were potential risk factors for severe periodontitis. The risk for periodontitis is considerably greater for tobacco users, with estimated ratios in the range of 2.5–7.0 or even higher for smokers as compared with nonsmokers. Even when the levels of plaque accumulation and gingival inflammation were not significantly different between smokers and nonsmokers, smokers exhibited an increase in prevalence as well as severity of destructive disease. The relationship between smoking and periodontitis appears to be dose-dependent; the odds for more severe attachment loss range from 2.05 for light smokers to 4.75 in heavy smokers, and there is a significant correlation between probing depth and smoking pack-years. Furthermore, years of exposure to tobacco products have been shown to be a statistically significant risk factor for periodontal disease in 1156 community dwelling New England elders, regardless of other social and behavioral factors.

In a study of 889 Spanish patients, gingival recession, probing depth, and clinical attachment level were significantly associated with smoking status. It was further noted that smoking one cigarette per day, up to 10, and up to 20, increased clinical attachment loss by 0.5%, 5% and 10%, respectively.

The data support those of Wouters et al.who found significantly less alveolar bone in individuals smoking more than 5 g of tobacco per day than in those smoking between 1 and 5 g of tobacco per day, as well as those of Norderyd and Hugoson, found that moderate to heavy smoking (greater than or equal to 10 cigarettes per day) was associated with severe periodontitis but light smoking (less than 10 cigarettes per day) was not. The response to surgical and nonsurgical periodontal treatment has been shown to be less favorable in smokers compared to nonsmokers in terms of probing depth reduction and clinical attachment gain, even in the presence of ongoing, effective supportive therapy. Furthermore, in a group of refractory periodontitis patients, 90% of the subjects reported to be smokers.

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